Clinical significance of genetic alteration in plasma of colorectal cancer patients

Lecomte, Thierry; Berger, A.; Zinzindouhoue, Frank; Micard, Stéphanie; Landi, Bruno; Beaune, Philippe; Cugnenc, Paul-Henri; Laurent‐Puig, Pierre

doi:10.1016/s0959-8049(01)80629-8

Cited by 2 publications

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“…Gene expression levels of the nucleotide excision repair gene, ERCC-1, may play a role in predicting survival time after oxaliplatin treatment for metastatic colorectal cancer [39]. A recent study has also demonstrated an association between the risk of oxaliplatin-induced cumulative neurotoxicity and polymorphisms in the genes encoding glutathione-S-transferases, a multigene family of enzymes involved in the metabolism of genotoxic compounds and their elimination [40]. These findings raise the possibility that patients at high risk for neuropathy may in the future be identified prior to the commencement of treatment and that individualization of dosing may help limit the extent of cumulative neuropathy.…”

Section: Incidence Of Oxaliplatin-induced Neuro-toxicitymentioning

confidence: 99%

The Pathophysiology of Oxaliplatin-Induced Neurotoxicity

Kiernan

Krishnan²

2006

CMC

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Nerve dysfunction is a common accompaniment of chemotherapy, typically occurring in a dose-dependent manner, so that the higher the dose and the longer the time of exposure, the more likely neuropathy is to occur. With the majority of chemotherapies, the mechanisms of neurotoxicity have not been clearly established. Cessation of therapy may prevent progression to a more severe syndrome and is often necessary even if there has been tumour response. Alternatively dose reduction may slow or halt progression. The clinical investigation of patients with suspected nerve dysfunction related to chemotherapy remains problematic. While routine nerve conduction studies can document the presence of a neuropathy, they do not provide further insight into pathophysiology. In contrast, measurements of nerve excitability by threshold tracking provide complementary information to conventional nerve conduction studies and may be used to infer the activity of a variety of ion channels, energy-dependent pumps and ion exchange processes activated during the process of impulse conduction. The present review will focus on recent developments in clinical rating scales and novel neurophysiological methods for the clinical investigation of chemotherapy-induced neurotoxicity, and will highlight how such methods may prove useful to study the neurological effects of chemotherapy. Specific emphasis will be placed on oxaliplatin, a platinum-based chemotherapy effective for colorectal cancer that exhibits dose-limiting neurotoxicity.

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Section: Incidence Of Oxaliplatin-induced Neuro-toxicitymentioning

confidence: 99%

The Pathophysiology of Oxaliplatin-Induced Neurotoxicity

Kiernan

Krishnan²

2006

CMC

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“…Previous studies revealed that GSTP1 Ile105Val substitution modifies the substrate affinity of the GSTP1 enzyme, and the homozygous Val105 variants may have altered substrate-dependent catalytic enzyme activity as compared to the Ile105 wildtype homozygous genotypes [7,8]. In particular, it was found that the GSTP1 105Val allele was more active in the metabolism in oxiplatin-based chemotherapy than the wildtype allele [9].…”

Section: Introductionmentioning

confidence: 99%

Glutathione S-Transferase Enzyme Polymorphisms in a Hungarian Myelodysplasia Study Population

Várkonyi

Szakály

Jánoskúti

et al. 2008

Pathol. Oncol. Res.

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GSTM1, GSTT1 and GSTP1 Ile105Val that are members of the GST gene family encode for Phase II drug/xenobiotic metabolizing enzymes, primarily with detoxifying function, and are polymorphic in humans. GSTM1 and GSTT1 homozygous deletion genotypes do not express the enzymes. It has been hypothesised that individuals with homozygous deletion of the GSTM1 and/or GSTT1 gene may have lower detoxification capacity towards genotoxic agents therefore those individuals may be at increased risk of myelodysplastic syndrome which is a preleukemic condition. Genetic polymorphism of GSTM1, GSTT1 and GSTP1 Ile105Val was investigated in a case-control study in a Hungarian patient population comprising 86 patients with myelodysplastic syndrome and 99 hospital-based controls. There were no statistically significant differences between cases and controls for the GSTM1, GSTT1 and GSTP1 Ile105Val genotype frequencies for any of the three genes separately and in various combinations. This suggests that these genetic polymorphisms may not be strong risk factors, if any, for myelodysplastic syndrome.

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Clinical significance of genetic alteration in plasma of colorectal cancer patients

Cited by 2 publications

References 0 publications

The Pathophysiology of Oxaliplatin-Induced Neurotoxicity

The Pathophysiology of Oxaliplatin-Induced Neurotoxicity

Glutathione S-Transferase Enzyme Polymorphisms in a Hungarian Myelodysplasia Study Population

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